Indeed, genomic profiling has revealed EBV+ tumours have a low mutational burden [32,105] and that mutations in MYD88-mediated TLR-signalling and B-cell receptor signalling pathways are less frequent in EBV+ DLBCL [106], unlike conventional ABC-like DLBCL [107,108]. This evidence concerns the gene MYD88 and diffuse large B-cell lymphoma.